This invention relates generally to medical intervention and, more particularly, to the treating of cardiac arrest patients, patients in various forms of shock and patients with head injury. More particularly, this invention relates to a method and apparatus for a non-invasive alteration of arterial blood pressures, myocardial and cerebral perfusion pressures, blood flow and cardiac output.
Approximately one million people per year have cardiac arrests in the United States. Less than 10% of these people are discharged from the hospital alive without neurological damage. This percentage of people discharged would be increased if the treatment available after the onset of cardiac arrest was improved. Areas in which this treatment could be improved include: (1) artificial circulation during cardiopulmonary resuscitation (CPR); (2) induction and maintenance of brief periods of cerebral hypertension after return of spontaneous circulation; and (3) continued circulatory support for the brain and heart after return of spontaneous circulation from cardiac arrest.
The blood of a cardiac arrest patient is artificially circulated during CPR by cyclically compressing the chest. One major theory describing how artificial circulation is generated during CPR states that compression of the chest causes global increases in intrathoracic pressure. This increase in intrathoracic pressure in the thoracic compartment is evenly distributed throughout the lungs and the four chambers of the heart, as well as the great vessels in the chest. The increase in thoracic pressure is greater than in the compartments above and below the chest. These compartments mainly include the neck and head above the chest and the abdominal compartment below the diaphragm and the chest. When thoracic pressure is increased above the pressure in these compartments, blood within the thoracic cavity moves to the head and abdomen with greater blood flow going toward the head. When the chest is released, the pressure within the thoracic cavity drops and becomes less than the pressure within the head and abdomen, therefore allowing blood to return to the thoracic cavity from the head and abdominal compartments. This theory of CPR-produced blood flow is termed the "thoracic pump mechanism," whereby the entire thorax itself acts as a pump with the heart itself acting as a passive conduit for blood flow. This theory is different from the cardiac pump mechanism, which states that compression of the chest produces blood flow by compressing the heart between the sternum and anterior structures of the vertebral column. In most patients, blood flow produced during chest compressions is likely a combination of the two theories. In each individual patient, blood flow during CPR depends on various factors, such as body habitus, with thinner individuals relying more on the cardiac pump mechanism of blood flow, and in larger individuals with increased anterior-posterior chest dimension relying on the thoracic pump mechanism. Both mechanisms of blood flow have been shown to be present in animal and human studies. Regardless of which mechanism is invoked, currently performed standard chest compressions as recommended by the American Heart Association produces 30% or less of the normal cardiac output. This results in extremely poor regional cerebral and myocardial blood flow during CPR. The level of blood flow generated during CPR is usually insufficient to re-start the heart and prevent neurologic damage. The purpose of CPR is to attempt to sustain the viability of the heart and brain until more definitive measures, such as electrical countershock and pharmacotherapy, are administered to the patient.
A main determinant for successful resuscitation from cardiac arrest is the coronary perfusion pressure produced during CPR. Coronary perfusion pressure (CPP) is defined as the aortic diastolic pressure minus the right atrial diastolic pressure. CPP represents the driving force across the myocardial tissue bed. Animal studies are plentiful which demonstrate that CPP is directly related to myocardial blood flow. It appears in humans that a CPP of at least 15 mm Hg is required for successful resuscitation. CPP of this magnitude is difficult to achieve with chest compressions alone. Patients, who utilize the thoracic pump mechanism for CPR, are even more unlikely to be able to produce this level of CPP during CPR alone. The major means for producing coronary perfusion pressures high enough for successful resuscitation have been to perform more forceful chest compressions and by administering various adrenergic agonists, such as epinephrine. Unfortunately, it has been shown that CPPs are difficult to augment with chest compressions alone and that in some situations very high doses of adrenergic agonists are required to produce higher CPPs. The difficulty in trying to produce higher CPPs with CPR alone lies in the fact that right atrial diastolic pressures are sometimes increased to the same or greater magnitude as aortic diastolic pressures. Using various adrenergic agonists, aortic diastolic pressure is usually augmented to a higher degree than right atrial diastolic pressure. However, the use of adrenergic agonists to achieve this have several drawbacks. These include increasing myocardial oxygen demands to a greater degree than can be met with blood flow produced during CPR. In addition, there are lingering effects of adrenergic agonists which may be detrimental after successful return of spontaneous circulation. These include periods of prolonged hypertension and tachycardia, which may further damage the heart and possibly cause re-arrest.
Cerebral perfusion pressure is a main determinant of cerebral blood flow. During cardiac arrest and CPR, autoregulation of blood flow in the brain may be lost. Cerebral perfusion pressure is defined as the mean arterial pressure minus the intracranial pressure. The main determinant of mean arterial pressure during CPR is aortic diastolic pressure. One of the main determinants of intracranial pressure during CPR is the mean venous pressure in the central circulation and the neck. Forward flow to the head is produced during CPR because of functional valves at the neck veins entering the thorax. These valves close during chest compressions, which prevent venous pressure transmission and flow of blood back into the neck and cranium. When these valves are not functioning, pressure is transmitted during the chest compression to the neck veins and into the cranium. This in effect decreases forward cerebral blood flow. Methods that increase cerebral blood flow during conventional CPR are mainly the use of adrenergic agonists. These agents selectively increase arterial pressure over venous pressure. Thus, mean arterial pressure becomes greater than intracranial and cerebral venous pressure thus producing net forward flow. However, use of adrenergic agonists have several drawbacks. In conventional doses, increases in cerebral blood flow are extremely variable with many individuals having no response at all. The use of higher doses of adrenergic agonists may be problematic as previously discussed under myocardial blood flow.
In summary, the major deficiencies in CPR-produced blood flow to the critical organs of the heart and brain are primarily due to the inability of conventionally performed CPR to cause highly selective increases in aortic diastolic pressure without causing increases of similar magnitude in central venous pressures. The ability to maximize the former while minimizing the latter would be extremely advantageous especially if the effects could be immediately reversed.
Several techniques have been developed to take advantage of the various CPR-produced mechanisms of blood flow. Two techniques that take advantage of the thoracic pump mechanism include simultaneous ventilation compression CPR (SVC-CPR) and vest-CPR. SVC-CPR is a technique that involves inflating the lungs simultaneously during the chest compression phase of CPR. This causes larger increases in intrathoracic pressure than external chest compression alone without ventilation or without external chest compression. This has been shown in animal studies to result in higher cerebral blood flows than in conventionally performed CPR. However, one major drawback is that coronary perfusion pressures are not uniformly increased and, in some instances, can be detrimentally decreased. When SVC-CPR was tested in a clinical trial, no increases in survival were noted over standard CPR.
Vest-CPR is a technique which utilizes a bladder containing vest analogous to a large blood pressure cuff and is driven by a pneumatic system. The vest is placed around the thorax of the patient. The pneumatic system forces compressed air into and out of the vest. When the vest is inflated, a relatively uniform decrease in circumferential dimensions of the thorax is produced which creates an increase in intrathoracic pressure. Clinically, the vest apparatus is cyclically inflated 60 times per minute with 100 mm Hg-250 mm Hg pressure which is maintained for 30%-50% of each cycle with the other portion of the cycle deflating the vest to 10 mm Hg. Positive pressure ventilation is performed independent of the apparatus after every fifth cycle. When studied clinically in humans, and compared with manually performed standard external CPR, the vest apparatus produced significantly higher coronary perfusion pressures and significantly higher mean aortic, peak aortic, and mean diastolic pressures. However, these changes are not uniformly seen in all patients. Of note, when the vest has been studied in the laboratory and clinical settings, larger doses of epinephrine have been used to achieve these higher coronary perfusion pressures since the thoracic pump model would predict aortic diastolic and right atrial diastolic pressures to be equivalent during the relaxation phase (when coronary perfusion occurs).
Another new technique, which takes some advantage of both the thoracic and cardiac pump mechanism of blood flow, is called "active compression/decompression CPR (ACDC-CPR)." This technique utilizes a plunger-type device, which is placed on the patient's sternum during cardiac arrest. The person performing chest compressions presses on the device which causes downward excursion of the anterior chest wall. The person then pulls up on the device. Since the device is attached to the sternum by suction, this causes the anterior chest to be actively recoiled instead of undergoing the usually passive recoil of standard external CPR. This active recoil is capable, in many individuals, of causing a decrease in intrathoracic pressure, which is transmitted to the right atrium thus lowering right atrial pressure during artificial diastole and, in turn, increasing coronary perfusion pressure. This negative right atrial pressure also has the effect of increasing venous return to the thoracic cavity, which may enhance cardiac output. Factors, such as body habitus and chest wall compliance, which impact on the efficacy of ACDC-CPR have not been studied, but are likely to have an effect. Persons with larger body habitus probably would receive less benefit from the technique.
Two other techniques, which are being investigated to resuscitate victims of cardiac arrest, and which do not rely on a mechanism of CPR-produced blood flow, include selective aortic arch perfusion and cardiopulmonary bypass. Both of these techniques require access to the central arterial vasculature. Selective aortic perfusion is experimental and involves percutaneously placing a balloon catheter in the aortic arch through a vessel, such as the femoral artery. The balloon catheter is placed in the aortic arch and the inflated balloon positioned just distal to the take-off of the carotid arteries. Perfusion takes place under pressure with oxygenated fluids or blood for various lengths of time. In this manner, the brain and heart are selectively perfused with little or no perfusion taking place distal to the occluded portion of the aorta. Over time, the central venous pressures will rise. This technique has not been tested clinically, but is expected to take a high level of expertise and cannot be readily performed in a setting outside of the hospital where many cardiac arrests occur.
Cardiopulmonary bypass during CPR is performed by obtaining central arterial and venous access usually percutaneously through the femoral artery and vein. This technique is capable of totally supporting the circulation by producing near normal cardiac outputs and blood flows to the heart and brain. Although shown to be effective, there are many technical difficulties which make its widespread use unfeasible. Large cannulas must be placed in the femoral artery and vein, which is difficult in the collapsed circulation. The bypass circuit is complicated and, if not properly primed, may produce air emboli. In addition, the patient requires systemic anticoagulation in most instances. The use of such a technique during CPR can be performed only at specially equipped centers with specially trained personnel.
Open-chest CPR is an old technique that was commonly performed before the advent of modern-day CPR. This technique involves opening the patient's chest by performing a thoracotomy. The descending aorta is usually cross-clamped. The heart itself is then manually massaged (compressed) with the hands. Although this technique is effective in producing heart and brain blood flows superior to standard CPR, it does not lend itself to widespread performance especially in the out-of-hospital setting. Reasons for this include the level of expertise required and the hazard of blood-borne pathogens. Other special equipment, such as the Anstadt cup, can be directly placed on the heart to mechanically compress the heart but, of course, have the same disadvantage of requiring a thoracotomy.
Two post-resuscitative interventions found to improve neurologic outcome in animal models of cardiac arrest is a brief period of immediate post-resuscitation hypertension and rapid induction and maintenance of cerebral hypothermia. The mechanisms for improved neurologic outcome with post-resuscitation hypertension is unclear. It is thought that this brief period of hypertension clears cerebral vessels of microthrombi, which may clog the cerebral circulation following cardiac arrest. It is also thought that this brief period of hypertension may help to prevent some of the post-resuscitation cerebral low flow and "no flow phenomenon," which contributes to neurologic injury. Post-resuscitation hypertension may decrease the overall amount of cerebral damage caused by cardiac arrest. One difficulty in providing for post-resuscitation hypertension is that the common means of producing this, through the use of adrenergic agonists, also produces considerable metabolic demands on the cardiovascular system.
Cardiogenic shock has many causes, including myocardial infarction, various forms of myocarditis, and other causes of myocardial injury. When severe, this condition becomes self-perpetuating secondary to the inability of the host to provide for adequate myocardial blood flow. This may result in further myocardial dysfunction leading to inadequate cerebral and myocardial blood flow and eventually to cardiac arrest. Cardiogenic shock may also be first noted after resuscitation from cardiac arrest depending on the length of the cardiac arrest. Cardiogenic shock may sometimes be difficult to distinguish from other forms of shock. Survival might be enhanced if myocardial and cerebral perfusion could be maintained until other definitive diagnostic and therapeutic measures could take place.
Immediate survival from cardiogenic shock will depend on maintenance of myocardial and cerebral blood flow. Various forms of treatment are available for cardiogenic shock, including various forms of pharmacotherapy and intra-aortic balloon pumping. Pharmacotherapy, while effective, requires invasive hemodynamic monitoring, such as pulmonary artery catheter placement for optimal titration. This may be difficult to institute in a timely manner when severe cardiogenic shock is first encountered especially in the pre-hospital setting. Intra-aortic balloon pumping in which a balloon catheter is placed into the thoracic aorta is effective but somewhat complicated to perform. Special equipment is needed for its placement and can only be performed at facilities which are capable of placing and maintaining such equipment and patients. Intra-aortic balloon pumping increases cardiac output by decreasing cardiac afterload. A balloon inflates during the diastolic portion of a cardiac cycle. This reduces cardiac afterload, thus lessening the workload on the heart. This balloon inflation during diastole also forces blood cephalad, thus perfusing the myocardial and cerebral tissues more effectively.
Other forms of shock, such as septic and neurogenic shock, cause hypoperfusion of critical organs due to a relative hypovolemia. Vascular tone is lost and requires a combination of volume replacement and vasopressors to maintain critical perfusion to vital organs. Immediate effective therapy aimed at maintaining cerebral and myocardial perfusion is difficult to institute because the various forms of shock are at times difficult to differentiate and therapy may differ between types of shock, although the immediate goal is to preserve myocardial and cerebral perfusion.
The major underlying immediate cause of death from any shock state is inadequate myocardial and cerebral perfusion. Survival with intact neurologic function is likely to be enhanced if myocardial and cerebral blood flow can be maintained until the underlying cause of the shock state can be optimally diagnosed and treated.
Head injury can be devastating. Much of the neurologic damage that takes place occurs after the initial insult. Blood flow to injured brain tissue is many times reduced below critical levels required to maintain survival when intracranial pressure is increased. Cerebral blood flow may be extremely difficult to maintain after the initial injury especially when multiple organ systems are involved in the trauma. Mean arterial blood pressure can also be difficult to maintain because of the ongoing blood loss into the thoracic and abdominal cavities or from extremity injuries. Intracranial pressure increases because of brain edema from the cerebral injury, or from expanding pools of blood from torn vessels in the brain or skull itself. Currently, the main mechanisms for reducing intracranial pressure involve the administration of diuretics, such as furosemide and mannitol, administration of steroids which reduce cerebral edema over time, removal of cerebral spinal fluid, elevation of the head which promotes venous drainage, administration of barbiturates which reduce the metabolic demand of brain tissue, hyperventilation producing hypocapnia and reduced cerebral blood flow which decreases intracranial pressure, and, as a last resort, removal of less necessary parts of the brain itself. Many of these therapies cannot be performed during the initial care of the multiple injured trauma patient who has both neurologic injury and multiple organ system injury, or have significant side effects. Administration of diuretics produce further volume depletion and may further reduce mean arterial pressure. Steroids require several hours to begin taking effect. Removal of cerebral spinal fluid and damaged brain tissue itself may take several hours to perform. Administration of barbiturates may also reduce the mean arterial pressure. Hyperventilation, although effective in reducing intracranial pressure, does so by decreasing cerebral blood flow which may be injurious to damaged tissue. All of these therapies become more complicated in the presence of other extra-cerebral organ injury. Occasionally, pharmacotherapy to raise mean arterial blood pressure is used to help maintain cerebral perfusion pressure in the face of rising intracranial pressure. This is difficult and sometimes dangerous to institute early because vasopressors many times increase the metabolic demands of other injured tissues.
Hemorrhagic shock is a leading cause of death from trauma. Many times there are delays in reaching hospitals which are qualified to take care of the complex injuries of such individuals. Many patients who die of trauma, die from multi-system involvement. Multi-system involvement may include head injury along with injuries to organs of the thoracic and abdominal cavity. Uncontrolled hemorrhage leading to hypovolemic shock is a leading cause of death from trauma especially from blunt and penetrating trauma of the abdomen. When head trauma occurs concomitantly with thoracic and abdominal hemorrhage, the brain becomes hypoperfused and, thus, becomes at greater risk for secondary injury. Currently, in the pre-hospital and emergency department setting, there are limited means to control exsanguinating hemorrhage below the diaphragm while maintaining myocardial and cerebral blood flow. Definitive control of hemorrhage is performed at surgery but this may be delayed and may not occur within the golden hour (time from injury to definitive treatment/repair) where the best opportunity lies in salvaging the patient. Survival with improved neurologic outcome might be enhanced if means were available to slow or stop ongoing hemorrhage (especially below the diaphragm) while maintaining adequate perfusion to the heart and brain until definitive treatment of the hemorrhage is available. This would be especially true of trauma victims whose transport to appropriate medical facilities would be prolonged.
The use of the pneumatic anti-shock garment (PASG) has met with varying degrees of success depending on the location of injury. This garment is placed on the legs and abdomen and is then inflated. Hemorrhage in the abdominal cavity, as well as the lower extremities, is controlled through tamponade while systemic blood pressure is raised partially through autotransfusion and by raising peripheral vascular resistance. Use of the PASG can sometimes be cumbersome and does not uniformly control hemorrhage or raise blood pressure. In addition, persons with concomitant penetrating thoracic injuries may hemorrhage more when the device is applied. The device may also raise intracranial pressure, which might detrimentally alter cerebral blood flow resulting in neurologic injury.
Other more drastic means to control abdominal bleeding prior to surgery have been the use of thoracotomy to cross-clamp the thoracic aorta and the use of balloon catheters placed into the aorta from the femoral arteries to a point above the celiac-aortic axis. These techniques have met with varying degrees of success and require a high degree of skill and cannot be performed in hospitals not equipped to care for trauma patients or by paramedical care personnel.
Deliberately keeping hemorrhaging trauma victims in a hypotensive state is currently being examined as a means to improve survival. This is done based on the premise that overall hemorrhage (especially abdominal hemorrhage) is reduced if mean arterial pressure is kept low by not aggressively volume-repleting the victim prior to surgery. Unfortunately, this may be dangerous for trauma victims with concomitant head injury or myocardial dysfunction.
An important cause of hemorrhagic shock not caused by trauma includes rupture of abdominal aortic aneurysms. These can occur suddenly and without warning. Control of bleeding even at surgery can be difficult. Temporary measures discussed above for hemorrhage secondary to trauma have been tried for hemorrhage secondary to aneurysm rupture. The same difficulties apply. Survival might be enhanced if hemorrhage could be controlled earlier while maintaining perfusion to the heart and brain.